It is the purpose of this study to findthe relation between protein synthesis, different types of myocardial stress, and ultimate cardiomyopaty which ensues. Cardiac stress due to hypertensive or volume overload will be induced in vitro in a young guinea pig or rabbit left ventricular perfusion model as well as in a right ventricular model in which coronary perfusion isunaltered despite the type of stress. The effects of anoxia, which coronary perfusion is unaltered despite the type of stress. The effects of anoxia, aging, and protein deficient diets on protein synthesis in these models will also be evaluated by utilizing labeled amino acids, measurements of their incorporation into proteins, and their intracellular or precursor pools. Sequetial changes leading to augmented or inhibited protein synthesis as adeylcyclase activity, nuclear polymerase activity, microsomal protein synthesis in cell free systems, RNA synthesis will be measured in hypertensive and volume overload. In addition, actin, myosin and its subunits, collagen, and myoglobin synthesis wll be measured in these stresses. The second main objective will attack the problem of cardiomyopathy in alcoholism or protein deficiencies by studying the effect of alcohol, its metabolite acetaldehyde, or protein deficient diets on protein synthesis in the perfused heart model. Questions to be asked include: (1) How do hypertensive or volume overloads trigger and stimulate increased protein synthesis? (2) Are the proteins snthesized in these stresses the same? (3) What is the effect of anoxia, aging and protein deficiency on the protein synthetic responses? (4) How do acetaldehyde or ethanol affect protein synthesis? (5) What therapeutic measures as increased oxygenation, glycosides, or specific amino acids will influence protein snthetic responses? Thus the rationale will be to findthe abnormal protein synthetic alteration in the varied stresses so that specific therapeutic measures may be taken to correct them.